The purpose of this research is to examine the role of and interaction between some vasoactive mediators in the regulation of fetal renal function and adaptation to extrauterine life. We proposed to investigate the effects of acute perinatal asphyxia on these control processes and to explore the possibility that profound asphyxia results in prolonged biological action of the vasoactive hormones. Our previous studies on the fetal lamb indicated that hypoxemia can cause profound disturbances in renal function and is a major stimulus for the release of catecholamines, renin-activity and vasopressin. These studies further indicated that the stress of labor and delivery also lead to increased plasma levels of these hormones, but that this rise is only partially explained by hypoxemia. Our current studies have shown that: (a) the high levels of VP observed during hypoxia in the fetus are far in excess of those required for maximal renal concentration and may therefore be involved in the maintenance of the circulation; (b) in addition to hypoxemia, acidemia as well as circulatory disturbances are contributing factors in stimulating the release of vasopressin; and (c) the fetus is as capable of eliminating vasopressin and norepinephrine as the newborn and adult and there is evidence of placental participation in their metabolisms.